A molecular basis for estrogen-induced cryptorchidism

In rodents, administration of DES during the second half of gestation resulted in a drastic reduction of Insl3 gene expression and testosterone levels, even though the expression of Sf-1 was unaltered

2000 Study Abstract

Male sexual differentiation relies upon testicular secretion of the hormones testosterone, Mullerian inhibiting substance, and insulin-3 (Insl3).

Insl3 is responsible for testicular descent through virilization and outgrowth of the embryonic gubernaculum.

In mouse, prenatal exposure to 17beta-estradiol and the nonsteroidal synthetic estrogen diethylstilbestrol (DES) disturbs the endocrine balance, causing demasculinizing and feminizing effects in the male embryo, including impaired testicular descent (cryptorchidism).

In the current study, we show that maternal exposure to estrogens, including 17alpha- and beta-estradiol, as well as DES, specifically down regulates Insl3 expression in embryonic Leydig cells, thereby providing a mechanism for cryptorchidism.

These experiments may have implications for the widespread use of estrogenic substances in agriculture and the environment.

Sources and more information
  • A molecular basis for estrogen-induced cryptorchidism, Developmental biology, NCBI PubMed PMID: 10926772, 2000 Aug.
  • Cryptorchidism in mice mutant for Insl3 featured image credit media.nature.
DES DIETHYLSTILBESTROL RESOURCES

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